The proposed research will examine the extent to which conflict over energy and resources between parent and offspring drives species diversification in plants. Specifically it will investigate whether seed lethality, which is a common outcome of hybridization in plants, results from conflicting interactions between maternal and paternal alleles over the allocation of nutritional resources to the developing embryo. This work will focus on two species of monkeyflower, Mimulus nudatus and Mimulus guttatus, which are not found to hybridize in the wild and can only be crossed with difficulty in the greenhouse. The work will take advantage of the cross compatibility that each of these species has to a third Mimulus species to introduce genes from the genome of one species into the genome of the other and observe the effect. This research will employ cutting-edge genomic sequencing techniques and novel statistical analyses of genomic data to identify and physically map candidate genes onto chromosomes that cause seed lethality in crosses between related species. The proposed experiments will test, using gene insertion techniques, what causal role these genes play in dysfunctional seed development. Finally, this project will examine whether maternal and paternal copies of genes are expressed at different levels in seeds, and whether abnormal expression patterns correlate with seed lethality. The proposed work represents an important contribution to our understanding of the genetic mechanisms underlying the process of species divergence in general. Moreover, it will enable us to characterize the function and diversity of genes causing failed hybridization between plants. This research has relevance both for our understanding of the factors driving plant diversification and for attempts to create new crop varieties from existing lines that usually cannot hybridize. PUBLIC HEALTH RELEVANCE: Genomic imprinting in mammals and plants represents a spectacular case of convergent evolution due to the shared trait of a physical connection between the developing embryo and the mother, and similar protein groups with multiple parallel actions are involved in both groups. In humans, disruptions in the normal process of genomic imprinting during development have been linked to neurological disorders, cardiovascular disease and metabolic disorders, including obesity. This research will increase our understanding of the genomic imprinting mechanisms involved in embryonic development and potentially lead to better tools for diagnosing and treating human diseases that arise from imprinting malfunction.